Sleep disorders are comorbid with most psychiatric disorders, but the link between these is not well understood. Neuroligin-2 (NLGN2) is a cell adhesion molecule that plays roles in synapse formation and neurotransmission. Moreover, NLGN2 has been associated with schizophrenia, but its implication in sleep remains unexplored. In the present thesis, the effect of Nlgn2 knockout (KO) on sleep architecture and EEG activity in mice has been investigated.
Two electroencephalography (EEG) electrodes were implanted above the right hemisphere in Nlgn2 KO mice and littermates to record EEG for four consecutive days. Vigilance states (wakefulness, rapid eye movement sleep [REM sleep], non-REM sleep [NREM sleep]) were identified on 4 sec epochs and vigilance state duration was calculated. Spectral analysis was performed on epochs without artifact using a Fast Fourier Transform.
Nlgn2 KO mice showed more wakefulness and less NREM and REM sleep compared to wild-type (WT) mice. The changes in wakefulness and sleep durations originated from alterations during the 12h dark period because KO mice exhibited normal sleep/wakefulness duration during the 12h light period. The relative power spectra showed a significant genotype effect for fast frequencies (25-50Hz) during all vigilance states, with KO mice having less activity than littermates. The KO mice exhibited increased spectral activity at 2-5 Hz during NREM sleep. Moreover, abnormal burst of EEG activity was identified in the KO mice during wakefulness and REM sleep.
These data suggest that NLGN2 participates in the regulation of sleep duration as well as EEG activity during wakefulness and sleep.